Skip to main content Skip to main navigation menu Skip to site footer

Hyperglycemia caused reduction of cortical bone thickness in streptozotocin-induced diabetic rat

Abstract

Background: Diabetes is a chronic metabolic disease characterized by hypergyclemia due to insulin deficiency (type 1 diabetes) or insulin insensitivity/resistance (type 2 diabetes). The significant metabolic changes that occur in diabetes also affect the skeleton and cause bone loss and/or altered bone matrix and strength, thereby increasing the risk of fracture. Hyperglycemia can alter cellular metabolic processes through the formation of advanced glycation end products (AGEs), which caused dysregulation of various cytokines as the underlying mechanism in the decrease of bone density. This study aimed to see the bone loss caused by hyperglycemia in rats, using cortical bone thickness as a parameter. Methods: This study was an analytical experimental study, which was conducted in a laboratory. The sample of this study was Wistar rat (Rattus norvegicus). Diabetes in the rats were induced using streptozotocin. The diabetic rats were then sacrificed 11 days later, and the left femur bone was obtanied. The bone was decalcified for 1 week, then prepared for histological slides. Cortical bone thickness was measured microscopically using Optilab Image Raster software at 10 different axis points, and then averaged. Results: The mean of cortical bone thickness were 32.43 ± 2.65 μm in the control (non diabetic) rats, and 26.64 ± 2.89 μm in streptozotocin-induced diabetic rats (p < 0.001). The diabetic rats had lower mean of cortical bone thickness than control by 5.79 μm. Conclusion: Cortical bone thickness in the diabetic rats were lower by 18% compared to control 11 days after induction of streptozotocin.

References

  1. Follak N, Klöting I, Wolf E, and Merk H. Delayed remodeling in the early period of fracture healing in spontaneously diabetic BB/OK rats depending on the diabetic metabolic state. Histol Histopathol. 2004; 19:473-486. http://www.hh.um.es/pdf/Vol_19/19_2/Follak-19-473-486-2004.pdf
  2. McCabe L, Zhang J, and Raehtz S. Understanding the skeletal pathology of type 1 and type 2 diabetes mellitus. Crit Rev Eukar Gene Expr. 2011; 21(2):187-206. http://doi.org/10.1615/CritRevEukarGeneExpr.v21.i2.70
  3. Larson SAM and Burns PR. The pathogenesis of Charcot neuroarthropathy: current concepts. Diabet Foot Ankle. 2012; 3:12236. http://doi.org/10.3402/dfa.v3i0.12236
  4. Garn SM, Poznanski AK, and Nagy JM. Bone Measurement in the Differential Diagnosis of Osteopenia and Osteoporosis. Radiology. 1971; 100(3):509-518. http://doi.org/10.1148/100.3.509
  5. Brandi ML. Microarchitecture, the key to bone quality. Rheumatology. 2009; 48:iv3-iv8. http://doi.org/10.1093/rheumatology/kep273
  6. Sood A, Cunningham C, and Lin S. The BB Wistar Rat as a Diabetic Model for Fracture Healing. ISRN Endocrinol. 2013; 2013:349604. http://doi.org/10.1155/2013/349604
  7. Purwanto B and Liben P. Model Hewan Coba untuk Penelitian Diabetes. 2014; Surabaya: PT Revka Petra Media.
  8. Zhang Q, Carlson J, Ke HZ, Li J, Kim M, Murphy K, et al. Dramatic Increase in Cortical Thickness Induced by Femoral Marrow Ablation Followed by a 3-Month Treatment with PTH in Rats. J Bone Miner Res. 2010; 25(6):1350-1359. http://doi.org/10.1002/jbmr.25
  9. Alblowi J, Kayal RA, Siqueria M, McKenzie E, Krothapalli N, McLean J, et al. High Levels of Tumor Necrosis Factor-α Contribute to Accelerated Loss of Cartilage in Diabetic Fracture Healing. Am J Pathol. 2009; 175(4):1574-1585. http://doi.org/10.2353/ajpath.2009.090148
  10. Wu Y, Xiao E, and Graves DT. Diabetes mellitus related bone metabolism and periodontal disease. Int J Oral Sci. 2015; 7:63-72. http://doi.org/10.1038/ijos.2015.2
  11. Kayal RA, Tsatsas D, Bauer MA, Allen B, Al-Sebaei MO, Kakar S, et al. Diminished Bone Formation During Diabetic Fracture Healing Is Related to the Premature Resorption of Cartilage Associated With Increased Osteoclast Activity. J Bone Miner Res. 2007; 22(4): 560-568. http://doi.org/10.1359/jbmr.070115
  12. Bab IA and Sela JJ. Cellular and Molecular Aspects of Bone Repair in Sela JJ and Bab IA (eds), Principles of Bone Regeneration pp 11-41. 2012; Secaucus, NJ: Springer. http://doi.org/10.1007/978-1-4614-2059-0_2
  13. Vestergaard P. Diabetes and Bone. J Diabetes Metab. 2011; S:1 http://doi.org/10.4172/2155-6156.S1-001
  14. Motyl KJ, McCabe LR, and Schwartz AV. Bone and Glucose Metabolism: A Two-Way Street. Arch Biochem Biophys. 2010; 503(1):2-10. http://doi.org/10.1016/j.abb.2010.07.030
  15. Abbassy MA, Watari I, and Soma K. The effect of diabetes mellitus on rat mandibular bone formation and microarchitecture. Eur J Oral Sci. 2010; 118(4):364-369. http://doi.org/10.1111/j.1600-0722.2010.00739.x

How to Cite

Wijaya, M. C., Sari, G. M., & Tinduh, D. (2017). Hyperglycemia caused reduction of cortical bone thickness in streptozotocin-induced diabetic rat. Bali Medical Journal, 6(1), 161–163. https://doi.org/10.15562/bmj.v6i1.393

HTML
0

Total
4

Share

Search Panel

Maria Cellina Wijaya
Google Scholar
Pubmed
BMJ Journal


Gadis Meinar Sari
Google Scholar
Pubmed
BMJ Journal


Damayanti Tinduh
Google Scholar
Pubmed
BMJ Journal